Camille Piguet1, Martin Desseilles2, Yann Cojan3, Virginie Sterpenich3, Alexandre Dayer4, Gilles Bertschy3, Patrik Vuilleumier4. 1. Department of Neuroscience, Faculty of Medicine, University of Geneva, 1206 Genève, Switzerland, Cyclotron Research Center, University of Liège, 4000 Liège, Belgium, Department of Psychiatry, Geneva University Hospital, 1205 Genève, Switzerland, Department of Psychiatry and Mental Health, Strasbourg University Hospital, University of Strasbourg, INSERMu1114, 67091 Strasbourg Cedex, France, and Department of Clinical Neuroscience, Geneva University Hospital, 1205 Genève, Switzerland camille.piguet@unige.ch. 2. Department of Neuroscience, Faculty of Medicine, University of Geneva, 1206 Genève, Switzerland, Cyclotron Research Center, University of Liège, 4000 Liège, Belgium, Department of Psychiatry, Geneva University Hospital, 1205 Genève, Switzerland, Department of Psychiatry and Mental Health, Strasbourg University Hospital, University of Strasbourg, INSERMu1114, 67091 Strasbourg Cedex, France, and Department of Clinical Neuroscience, Geneva University Hospital, 1205 Genève, Switzerland Department of Neuroscience, Faculty of Medicine, University of Geneva, 1206 Genève, Switzerland, Cyclotron Research Center, University of Liège, 4000 Liège, Belgium, Department of Psychiatry, Geneva University Hospital, 1205 Genève, Switzerland, Department of Psychiatry and Mental Health, Strasbourg University Hospital, University of Strasbourg, INSERMu1114, 67091 Strasbourg Cedex, France, and Department of Clinical Neuroscience, Geneva University Hospital, 1205 Genève, Switzerland Department of Neuroscience, Faculty of Medicine, University of Geneva, 1206 Genève, Switzerland, Cyclotron Research Center, University of Liège, 4000 Liège, Belgium, Department of Psychiatry, Geneva University Hospital, 1205 Genève, Switzerland, Department of Psychiatry and Mental Health, Strasbourg University Hospital, University of Strasbourg, INSERMu1114, 67091 Strasbourg Cedex, France, and Department of Clinical Neuroscience, Geneva University Hospital, 1205 Genève, Switzerland. 3. Department of Neuroscience, Faculty of Medicine, University of Geneva, 1206 Genève, Switzerland, Cyclotron Research Center, University of Liège, 4000 Liège, Belgium, Department of Psychiatry, Geneva University Hospital, 1205 Genève, Switzerland, Department of Psychiatry and Mental Health, Strasbourg University Hospital, University of Strasbourg, INSERMu1114, 67091 Strasbourg Cedex, France, and Department of Clinical Neuroscience, Geneva University Hospital, 1205 Genève, Switzerland. 4. Department of Neuroscience, Faculty of Medicine, University of Geneva, 1206 Genève, Switzerland, Cyclotron Research Center, University of Liège, 4000 Liège, Belgium, Department of Psychiatry, Geneva University Hospital, 1205 Genève, Switzerland, Department of Psychiatry and Mental Health, Strasbourg University Hospital, University of Strasbourg, INSERMu1114, 67091 Strasbourg Cedex, France, and Department of Clinical Neuroscience, Geneva University Hospital, 1205 Genève, Switzerland Department of Neuroscience, Faculty of Medicine, University of Geneva, 1206 Genève, Switzerland, Cyclotron Research Center, University of Liège, 4000 Liège, Belgium, Department of Psychiatry, Geneva University Hospital, 1205 Genève, Switzerland, Department of Psychiatry and Mental Health, Strasbourg University Hospital, University of Strasbourg, INSERMu1114, 67091 Strasbourg Cedex, France, and Department of Clinical Neuroscience, Geneva University Hospital, 1205 Genève, Switzerland.
Abstract
OBJECTIVES: Thought disorders such as rumination or flight of ideas are frequent in patients with mood disorders, and not systematically linked to mood state. These symptoms point to anomalies in cognitive processes mediating the generation and control of thoughts; for example, associative thinking and inhibition. However, their neural substrates are not known. METHOD: To obtain an ecological measure of neural processes underlying the generation and suppression of spontaneous thoughts, we designed a free word association task during fMRI allowing us to explore verbal associative patterns in patients with mood disorders and matched controls. Participants were presented with emotionally negative, positive or neutral words, and asked to produce two words either related or unrelated to these stimuli. RESULTS: Relative to controls, patients produced a reverse pattern of answer typicality for the related vs unrelated conditions. Controls activated larger semantic and executive control networks, as well as basal ganglia, precuneus and middle frontal gyrus. Unlike controls, patients activated fusiform gyrus, parahippocampal gyrus and medial prefrontal cortex for emotional stimuli. CONCLUSIONS: Mood disorder patients are impaired in automated associative processes, but prone to produce more unique/personal associations through activation of memory and self-related areas.
OBJECTIVES: Thought disorders such as rumination or flight of ideas are frequent in patients with mood disorders, and not systematically linked to mood state. These symptoms point to anomalies in cognitive processes mediating the generation and control of thoughts; for example, associative thinking and inhibition. However, their neural substrates are not known. METHOD: To obtain an ecological measure of neural processes underlying the generation and suppression of spontaneous thoughts, we designed a free word association task during fMRI allowing us to explore verbal associative patterns in patients with mood disorders and matched controls. Participants were presented with emotionally negative, positive or neutral words, and asked to produce two words either related or unrelated to these stimuli. RESULTS: Relative to controls, patients produced a reverse pattern of answer typicality for the related vs unrelated conditions. Controls activated larger semantic and executive control networks, as well as basal ganglia, precuneus and middle frontal gyrus. Unlike controls, patients activated fusiform gyrus, parahippocampal gyrus and medial prefrontal cortex for emotional stimuli. CONCLUSIONS:Mood disorderpatients are impaired in automated associative processes, but prone to produce more unique/personal associations through activation of memory and self-related areas.
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